The primary goal of this project is to determine how the central auditory system reorganizes functionally and structurally as a result of temporary or permanent injury to the cochlea. The first objective of the project will determine how the discharge patterns of single neurons in the cochlear nucleus (CN) and central nucleus of the inferior colliculus (ICC) are altered by acoustic overstimulation that causes temporary threshold shift (TTS) or permanent threshold shift (PTS). A second objective of the project will determine if there is any evidence of axonal sprouting, as reflected in GAP-43 immunohistochemistry, in the CN or IC as a result of chronic cochlear lesions. The project aims to answer the following questions. How is the tonotopic organization of the CN and ICC altered by PTS and cochlear lesions. Is the tonotopic map reorganized or is there a "silent region' in the ICC or CN corresponding to the region of cochlear damage? How are the excitatory and inhibitory response areas of units in the CN and ICC altered by TTS and PTS. Is there a change in the best frequency or width of the excitatory or inhibitory response areas when either the excitatory or inhibitory response area is selectively damaged or inactivated? Does the saturation firing rate and the dynamic range of a unit increase or decrease when the injury is confined to either the excitatory or inhibitory response area? Are the functional changes in the CN and ICC related to the pattern of cell damage in the cochlea or the compound action potential threshold shift? Do cochlear lesions give rise to increased levels of GAP-43 immunostaining, indicative of axonal sprouting, in the CN or ICC? Is the spatial distribution of GAP-43 immunostaining within the ICC or CN related to the location of the cochlear lesion? The results of the project should provide new insights regarding the structural and functional plasticity of the central auditory pathway following chronic or acute injury to the periphery. Moreover, the data may provide a clearer understanding of the neural mechanisms underlying many of the symptoms of sensorineural hearing loss such as loudness recruitment, tinnitus, poor speech discrimination and diplacuis. Finally, the functional changes may provide new information related to the underlying neural circuits present in the ICC and CN.